Galectin-1在膀胱癌细胞中的表达及其对膀胱癌细胞增殖和迁移能力的影响

Expression of Galectin-1 in bladder cancer cells and its impact on proliferation and migration of bladder cancer cells

目的检测膀胱癌细胞中半乳糖凝聚素1(Gal-1)的表达是否异常,并通过慢病毒干扰技术敲除膀胱癌细胞中Gal-1的表达后,检测肿瘤细胞的增殖能力与迁移能力有无改变。方法用荧光实时定量聚合酶链锁反应(q RT-PCR)和蛋白质印迹法(Western Blot)技术分别检测膀胱癌细胞与正常膀胱上皮细胞相比,Gal-1的表达在m RNA水平以及蛋白水平有无区别。再利用RNA干扰慢病毒敲除膀胱癌细胞内Gal-1的表达后,通过WST-1试剂盒以及transwell迁移实验检测膀胱癌细胞的增殖和迁移能力有无发生改变。最后再应用Western Blot技术检测敲除Gal-1的表达后AKT、P38、JNK三条通路的激活水平有无发生改变。结果膀胱癌细胞内的Gal-1的表达水平与正常膀胱上皮细胞相比,无论在m RNA水平还是在蛋白水平均明显上调。敲除Gal-1的表达后肿瘤细胞的增殖能力未发生明显改变,但迁移能力明显下调。敲除Gal-1的表达后,AKT信号通路的磷酸化水平明显下降。结论 Gal-1在膀胱癌细胞中表达明显上调,并且与膀胱癌细胞的迁移能力密切相关。Gal-1可能通过改变AKT信号通路的激活水平从而调控了膀胱癌细胞的迁移能力。

【Objective】To explore the expression of Galectin-1（Gal-1） in bladder cancer cells and study whether the proliferation and migration of bladder cancer cells will be changed after knocking down the expression of Gal-1 in bladder cancer cells using RNA interfere lentivirus.【Methods】The different expression of Gal-1 between bladder cancer cells and normal transitional cells was examined by quantitative real time polymerase chain reaction（q RT-PCR） and western blot（WB）, respectively. After knocking down the expression of Gal-1 in cancer cells by lentivirus-mediated RNA interference, WST-1 assays and transwell system would be used to research the proliferation and migration of bladder cancer cells. In addition, the activation of AKT, P38, and JNK signal pathway after knocking down the expression of Gal-1 were tested by WB.【Results】Compared with the normal human urothelium cells, the expression of Gal-1 in bladder cancer cells obviously elevated in both m RNA and protein levels. After knocking down the expression of Gal-1, the proliferation of bladder cancer cells was comparable between RNA interfere group and control groups, while the migration of bladder cancer cells weakened in Gal-1 interfere group. Moreover, the phosphorylation of AKT signal pathway dropped off, with Gal-1 knocked down in bladder cancer cells.【Conclusion】Gal-1 was overexpressed in bladder cancer cells and it played an important role in the mobility and migration of bladder cancer cells. Gal-1 may regulate the mobility and migration ability of bladder cancer cells by altering the activation level of AKT signaling pathway.